Chronic cigarette smoke exposure adversely alters 14C-arachidonic acid metabolism in rat lungs, aortas and platelets

Lubawy, William C.; Valentovic, Monica; Atkinson, John; Gairola, Gary

doi:10.1016/0024-3205(83)90133-9

Cited by 21 publications

(2 citation statements)

References 17 publications

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“…Several of these mechanisms could have acted together to induce the activation of leucocyte/endothelium interaction by cigarette smoke (3, 13-15, 26, 30). Finally, cigarette smoke exerts peroxidative damage to endothelial cells, leading to reduced generation of antiadhesive prostacyclin (16), increased adhesion of platelets (19), endothelial cell swelling, opening of endothelial junctions, extravasation of uid and macromolecules, and formation of subendothelial oedema.…”

Section: Discussionmentioning

confidence: 99%

In Vivo Evaluation of Leucocyte Dynamics in Cremaster Muscle in Rats After Exposure to Cigarette Smoke

Chen

Lee

Wei

et al. 2002

Scandinavian Journal of Plastic and Reconstructive Surgery and

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This experiment was designed to examine the effects of chronic cigarette smoking on the microcirculation immediately after exposure to smoke for two, four, and six weeks and after withholding smoke for two weeks from those previously exposed for four weeks. The mean (SD) rolling leucocytes at two, four, and six weeks were 11.10 (1.8), 23.7 (2.3), 40.2 (3.9) (p < 0.001). The rolling leucocytes after smoking for four weeks and then having smoke withheld for two weeks was 9.6 (1.4). The mean adherent leucocytes were 5.0 (0.7), 7.5 (1.1), 12.6 (1.8) (p < 0.001). The adherent leucocytes after smoking for four weeks and then having smoke withheld for two weeks was 3.5 (0.5). Our results confirm those of many previous studies of the adverse effects of cigarette smoking, and also that those deleterious effects are time-dependent. The reversibility of the deleterious effect of cigarette smoking after cessation of cigarette smoking before face-lift or flap reconstruction is at least two weeks. This information is also important for clinical management of patients who smoke and who are scheduled for face-lift and flap reconstruction. Two weeks without cigarettes is a necessary period for successful elective plastic surgery.

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Section: Discussionmentioning

confidence: 99%

In Vivo Evaluation of Leucocyte Dynamics in Cremaster Muscle in Rats After Exposure to Cigarette Smoke

Chen

Lee

Wei

et al. 2002

Scandinavian Journal of Plastic and Reconstructive Surgery and

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“…These eicosanoids have profound physiological, biochemical and immunological effects, suggesting that lungs may play an important role in many biological functions mediated by eicosanoids (1,4,5). Prostaglandin synthesis in lungs is affected by several factors, including drugs (6), antioxidants (7), radiation (8) and cigarette smoke (9). There is also marked variation in the type and quantity of prostaglandins synthesized in lungs of different species (10,11).…”

Section: Introductionmentioning

confidence: 99%

Lipid composition and prostaglandin synthesis in mouse lung microsomes: Alterations following the ingestion of menhaden oil

Lokesh

Kinsella

1985

Lipids

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Three groups of male mice were fed a normal diet or a semisynthetic diet containing either 10% hydrogenated coconut oil (CO group) or 10% menhaden oil (MO group) for two wk. The synthetic diet altered the fatty acid composition of lung microsomal lipids. Mice ingesting menhaden oil contained greater amounts of eicosapentaenoic acid (20:5 n-3), docosapentaenoic acid (22:5 n-3) and docosahexaenoic acids (22:6 n-3) and decreased amounts of n-6 fatty acids such as arachidonic and adrenic. Synthesis of prostaglandin E2 and prostaglandin F2 alpha from exogenous arachidonic acid was significantly depressed in n-3 fatty acid-enriched lung microsomes. These studies indicated that dietary fish oil not only alters the fatty acid composition of lung microsomes but also lowers the capacity of lungs to synthesize prostaglandins from arachidonic acid.

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Changes of diastolic function induced by cigarette smoking: An echocardiographic study in patients with coronary artery disease

Störk¹,

Eichstädt

Möckel

et al. 1992

Clinical Cardiology

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Summary:In 28 chronic smokers (1 1 women, 17 men, 53 k 10 years old) with coronary artery disease (>75% stenosis), left ventricular (LV) relaxation and filling behavior was assessed before and after inhalation of 0.9 mg nicotine (1 cigarette) by echocardiography. The following acute nicotine-mediated changes were noted (one-sided Wilcoxon test): heart rate increased from 67 to 81 beatshin (p>.OOl); the early diastolic flow (E wave) integral decreased from 49 to 39 mm (p<.OOl); the late diastolic flow integral (A wave) increased from 36 to 41 mm (p<.Ol). Consecutively, the ratio between E and A wave flow integrals decreased from 1.4 to 0.9 (p< .OOl); the atrial contribution to LV filling rose from 42 to 53% (p<.OOl); and the isovolumetric relaxation period increased from 89 to 122 ms (p<.OOl). In cigarette smokers with coronary artery disease acute administration of nicotine hence causes a shift of mitral blood flow from early (E wave) to late (A wave) diastole and a prolongation of the isovolumetric relaxation time. Thus, cigarette smoking significantly affects LV diastolic function independently of its role as a risk factor for coronary atherosclerosis.

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Chronic cigarette smoke exposure adversely alters 14C-arachidonic acid metabolism in rat lungs, aortas and platelets

Cited by 21 publications

References 17 publications

In Vivo Evaluation of Leucocyte Dynamics in Cremaster Muscle in Rats After Exposure to Cigarette Smoke

In Vivo Evaluation of Leucocyte Dynamics in Cremaster Muscle in Rats After Exposure to Cigarette Smoke

Lipid composition and prostaglandin synthesis in mouse lung microsomes: Alterations following the ingestion of menhaden oil

Changes of diastolic function induced by cigarette smoking: An echocardiographic study in patients with coronary artery disease

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